ライフサイエンスコーパス: lymphovascular

1 uently changed elements were grade (40%) and lymphovascular (26%), nodal (15%), and margin (12%) stat

2 This organ-specific lymphovascular abnormality can be rescued by allowing em

3 Spheroidgenesis and lymphovascular emboli formation are the direct result of

4 BC xenograft, MARY-X, which manifests florid lymphovascular emboli in severe combined immunodeficient

5 This model exhibited lymphovascular emboli in vivo and corresponding spheroid

6 alence of xenograft-generated spheroids with lymphovascular emboli in vivo with both structures demon

7 This Notch 3 addiction of lymphovascular emboli might be exploited in future thera

8 xhibited by MARY-X also was exhibited by the lymphovascular emboli of human IBC cases independent of

9 The lymphovascular emboli of human IBC exhibited dual N3icd

10 jected i.v. immunolocalized to the pulmonary lymphovascular emboli of MARY-X and caused their dissolu

11 ere only weakly tumorigenic and did not form lymphovascular emboli.

12 ysis of E-cad generates the formation of the lymphovascular embolus and is responsible for its unique

13 adherin overexpression in the genesis of the lymphovascular embolus of IBC.

14 However, within the lymphovascular embolus, E-cad and its proteolytic proces

15 [hazard ratio (HR) = 1.8; 95% CI, 1.2-2.8], lymphovascular invasion (HR = 2.2; 95% CI, 1.4-3.4), and

16 o test the significance of adding grade (G), lymphovascular invasion (L), estrogen receptor (ER) stat

17 that bladder cancer patients with associated lymphovascular invasion (LVI) are at increased risk of o

18 Lymphovascular invasion (LVI) was the only clinicopathol

19 in situ (DCIS), invasive carcinoma (IC), or lymphovascular invasion (LVI), and 8% lobular neoplasia

20 ow thickness, mitotic rate (MR), ulceration, lymphovascular invasion (LVI), and regression; incidence

21 SBE] and long segment [LSBE]), nodal status, lymphovascular invasion (LVI), and the presence of multi

22 adverse prognostic factors are younger age, lymphovascular invasion (LVI), high Ki-67, and larger tu

23 eceptor status, HER2/neu status, presence of lymphovascular invasion (LVI), number of SLN(s) identifi

24 cinoma (IBC) is characterized by exaggerated lymphovascular invasion (LVI), recapitulated in our huma

25 eals a 1.5 cm IDC that is high grade without lymphovascular invasion (LVI).

26 r emboli within lymphovascular spaces termed lymphovascular invasion (LVI).

27 and significantly higher in the presence of lymphovascular invasion (LVI; 0.25 +/- 0.02 v 0.17 +/- 0

28 nodal metastasis (OR, 3.400; P = 0.017) and lymphovascular invasion (OR, 3.055; P = 0.045).

29 ted with grade 3 tumors (P = .0007) and with lymphovascular invasion (P < .0001).

30 ated with poor differentiation (P = 0.0015), lymphovascular invasion (P < 0.0001), and tumor size >/=

31 merican Joint Committee on Cancer stage, and lymphovascular invasion (P < 0.0001, P < 0.0001, P = 0.0

32 alysis showed that tumor number (P < 0.001), lymphovascular invasion (P < 0.001), and poor differenti

33 Lymph node metastases (P < 0.001), lymphovascular invasion (P < 0.001), and the presence of

34 reslow thickness (P = 0.012) and presence of lymphovascular invasion (P = 0.018) were the only factor

35 rentiated tumors (P = 0.004) and presence of lymphovascular invasion (P = 0.031).

36 nt (P<.001), infiltrative growth (P=.01), or lymphovascular invasion (P=.01).

37 The presence of lymphovascular invasion and clinically, but not microsco

38 -dimer, is a clinically important marker for lymphovascular invasion and early tumor metastasis in op

39 ll-differentiated invasive carcinoma without lymphovascular invasion and intermediate grade ductal ca

40 d it was an independent predictive marker of lymphovascular invasion and lymph node involvement.

41 sion was associated with muscle, neural, and lymphovascular invasion and the presence and number of i

42 ivariate analysis, pathologic response >95%, lymphovascular invasion and/or perineural invasion (PNI)

43 r receptor 2 (HER2) status, tumor grade, and lymphovascular invasion are relevant; Oncotype DX score

44 The step of intravasation or lymphovascular invasion can be a rate-limiting step in t

45 I tumors, although markers such as grade and lymphovascular invasion did not add value in this subset

46 Importantly, only 1 of 132 patients without lymphovascular invasion died of MCC.

47 might shed light on the general mechanism of lymphovascular invasion exhibited by all metastasizing c

48 carcinoma manifests an exaggerated degree of lymphovascular invasion in situ; hence, a study of its m

49 ted D-dimer levels predicted the presence of lymphovascular invasion in univariate logistic regressio

50 is cohort, especially among patients showing lymphovascular invasion on biopsy.

51 ents with T2-3, N0 rectal cancers and either lymphovascular invasion or elevated CEA levels have redu

52 High-risk (lymphovascular invasion positive) patients with CS1 NSGC

53 gative, PgR-negative, HER2-negative) tumors, lymphovascular invasion positivity, or estimated distant

54 sis (2 factors: HR, 4.1 [95% CI, 1.0-16.6]), lymphovascular invasion predicted death from disease (HR

55 ent age, tumor size, palpability, grade, and lymphovascular invasion predicted lymph node status.

56 riate analysis, patient age, tumor size, and lymphovascular invasion remained significant.

57 Lymphovascular invasion was the only significant factor

58 Pathologic stage and lymphovascular invasion were independent predictors of D

59 easing Clark level, mitoses, ulceration, and lymphovascular invasion were independently associated wi

60 ge, pN stage, LNR >/=0.2, tumor grade 3, and lymphovascular invasion were significantly associated wi

61 The step of intravasation (lymphovascular invasion), a rate-limiting step in metast

62 e receptor, nuclear grade, histologic grade, lymphovascular invasion, and clinical stage grouping) we

63 h tumor size, depth of invasion, presence of lymphovascular invasion, and degree of tumor differentia

64 C can be used for prediction of tumor grade, lymphovascular invasion, and depth of myometrial invasio

65 Tumors that had poor differentiation, lymphovascular invasion, and size >/=2 cm were significa

66 h of tumor invasion, tumor size, presence of lymphovascular invasion, and tumor grade.

67 ed progression and cancer-specific survival (lymphovascular invasion, associated carcinoma in situ, n

68 or age, race, stage, grade, receptor status, lymphovascular invasion, body mass index, diabetes, hype

69 d clear margins; grade 3 tumour histology or lymphovascular invasion, but not both, were permitted),

70 Plasma D-dimer levels were markers of lymphovascular invasion, clinical stage, and lymph node

71 logical level, the depth of tumour invasion, lymphovascular invasion, invasion of large veins, host l

72 isease without receipt of endocrine therapy, lymphovascular invasion, multifocal disease on pathology

73 absence of chronic kidney disease, negative lymphovascular invasion, negative surgical margin, and a

74 advanced pathologic stage, low-lying tumor, lymphovascular invasion, or perineural invasion.

75 statectomy Gleason sum, lymph node invasion, lymphovascular invasion, perineural invasion, and higher

76 umbers of positive and negative lymph nodes, lymphovascular invasion, perineural invasion, and use of

77 e, histologic type, tumor size, tumor grade, lymphovascular invasion, perineural invasion, type of op

78 Lymphovascular invasion, preoperative serum carcinoembry

79 ient age, tumor grade, clinical tumor stage, lymphovascular invasion, resection margin status, and su

80 ned immunodeficient mice without manifesting lymphovascular invasion, this step has been difficult to

81 Age, tumor size, tumor type, lymphovascular invasion, tumor location, multifocality,

82 Lymphovascular invasion, tumor size >/=2 cm, and poor di

83 f breast cancer characterized by exaggerated lymphovascular invasion, which is a phenotype recapitula

84 7%/3% of seminoma recurrences, in 48%/38% of lymphovascular invasion-negative and 41%/61% of lymphova

85 ovascular invasion-positive CSI nonseminoma, lymphovascular invasion-negative CSI nonseminoma and CSI

86 nths) and 14 months (range, 2-84 months) for lymphovascular invasion-positive CSI nonseminoma, lympho

87 phovascular invasion-negative and 41%/61% of lymphovascular invasion-positive patients, respectively.

88 osis between tumor grade and the presence of lymphovascular invasion.

89 r emboli within lymphovascular spaces called lymphovascular invasion.

90 There was extensive lymphovascular invasion.

91 breast carcinomas correlates with increased lymphovascular invasion.

92 e, MMR, number of nodes examined, grade, and lymphovascular invasion.

93 inoma, poorly differentiated (grade 3), with lymphovascular invasion.

94 ller median size, and less frequently showed lymphovascular invasion.

95 are locally invasive and exhibit peritumoral lymphovascular invasion.

96 le to, or greater than, tumor size, grade or lymphovascular invasion.

97 term disease-free survival in the absence of lymphovascular invasion.

98 T1b, non-high nuclear grade tumors, without lymphovascular invasion.

99 ocation, or multicentricity; the presence of lymphovascular invasion; histologic or nuclear grade; or

100 prognosis depends on the depth of invasion, lymphovascular involvement, and histological type.

101 e, location,and differentiation, presence of lymphovascular or perineural invasion,mucinous histology

102 logic stage, tumor distance from anal verge, lymphovascular or perineural invasion.

103 ssion analysis showed that stage III cancer, lymphovascular permeation, and blood transfusion, but no

104 pendent of age, sex, pathological stage, and lymphovascular space invasion (coefficient 9.81, 95% CI

105 multifocal pattern of residual disease, and lymphovascular space invasion in the specimen.

106 than 2 cm, multifocal residual disease, and lymphovascular space invasion predict higher rates of LR

107 ed with tumor histology, primary tumor size, lymphovascular space invasion, extranodal extension, the

108 sociated with higher grade and more frequent lymphovascular space invasion.

109 have higher-grade cancers and more frequent lymphovascular space invasion.

110 ctors (subtype, tumour grade, involvement of lymphovascular space), disease stage (including myometri

111 margin of invasive ductal carcinomas, in the lymphovascular space, and in lymph node metastases.

112 characterized by florid tumor emboli within lymphovascular spaces called lymphovascular invasion.

113 characterized by florid tumor emboli within lymphovascular spaces termed lymphovascular invasion (LV

114 lymphangiomas, congenital hamartomas of the lymphovascular tissue, are often associated with signifi

115 The genesis and unique properties of the lymphovascular tumor embolus are poorly understood large

116 The lymphovascular tumor embolus is a blastocyst-like struct